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RHEUMATOIDARTHRITIS,OSTEOARTHRITIS
GOUT,SPONDILITIS
 Rheumatoid arthritis (RA) is a chronic
systemic inflammatory disease predominantly
affecting diarthrodial joints and frequently a
variety of other organs.
 Peak incidence is between 4th and 6th decade.
 Females are two to three times more affected
than males.
 Genetic and autoimmune factors are mainly
responsible for the initiation of disease
process.
The pathologic hallmark of RA is synovial
membrane proliferation and outgrowth
associated with erosion of articular
cartilage and subchondral bone.
There is role of both cellular and
humoral immune mechanism in the
onset of inflammation.
 Small joints of Hand-Pain/Stiffness > 1HR.
 The pattern of joint involvement is typically
polyarticular and symmetrical and involves-
 proximal interphalangeal (PIP)
 metacarpophalangeal (MCP)
 wrist, elbow, shoulder, knee, ankle,MTP joints
and cervical spine.
 The distal interphalangeal (DIP) joints of the
fingers are usually spared.
 FEVER/MALAISE/HEADACHE
 JOINT SWELLING/TENDERNESS.
 With persistent inflammation, a variety of
characteristic joint changes develop like-
 Z-deformity
 Swan neck deformity
 Boutonniere deformity.
 CLINICAL.
 MRI IOC for early detection of
disease
 ULTRASOUND
 X-RAYS.
 CT SCAN.
 SYNOVIAL FLUID ASPIRATION
 ANEMIA,RAISED ESR…
 SEROLOGICAL TESTS.
 Guidelines for classification
 a. Four of seven criteria are required to classify
a patient as having rheumatoid arthritis (RA).
 b. Patients with two or more clinical diagnoses
are not excluded.
 Criteria
a. Morning stiffness: Stiffness in and around the
joints lasting 1 h before maximal improvement.
b. Arthritis of three or more joint areas: The 14
possible joint areas involved are right or left
proximal interphalangeal, metacarpophalangeal,
wrist, elbow, knee, ankle, and
metatarsophalangeal joints.
c. Arthritis of hand joints: Arthritis of wrist,
metacarpophalangeal joint, or proximal
interphalangeal joint.
d. Symmetric arthritis: Simultaneous
involvement of the same joint areas on both
sides of the body.
e. Rheumatoid nodules: Subcutaneous nodules
over bony prominences, extensor surfaces, or
juxtaarticular regions observed by a physician.
f. Serum rheumatoid factor: Demonstration of
abnormal amounts of serum rheumatoid factor.
g. Radiographic changes: Typical changes of
RA on posteroanterior hand and wrist
radiographs that must include erosions or
unequivocal bony decalcification localized in or
most marked adjacent to the involved joints.
 Most common type of arthritis.
 Leading cause of disability in elderly.
 Much more common in women than men.
 Definition: OA is joint failure,a disease in
which all parts of joint have undergone
pathologic change.initial step in the onset of
disease is failure of joint protective mechanism.
 Joint vulnerability and joint loading are the two
major factors in development of disease.
Primary osteoarthritis is mostly related to aging. With aging, the
water content of the cartilage increases, and the protein makeup
of cartilage degenerates.
Secondary osteoarthritis is caused by another disease or
condition. Conditions that can lead to secondary osteoarthritis
include obesity, repeated trauma or surgery to the joint structures,
abnormal joints at birth (congenital abnormalities), gout, diabetes,
and other hormone disorders.
 Increasing age.
 Female gender.
 Obesity
 Injurious physical activity.
 Bridging muscle weakness.
 Malalignment.
 Proprioceptive deficiancies(eg.charcot
arthropathy).
 Genetic susceptibility.(hand and hip OA.)
 Cartilage is the primary target tissue for OA.
 There is nonuniform loss of the cartilage.
 Evidense of new bone formation is presence of
osteophytes.
 There is as assymetric and nonuniform
involvement of the joints.
 Capsule may become edematous and fibrotic.
 Joint space narrowing is present as seen in all
types of arthritis.
Symptoms
Pain
o Joints may ache, or the pain may feel burning or sharp. For some people, it may get
better after a while.
o Pain while sleeping or constant pain may be a sign that arthritis is getting worse.
Stiffness
o When you have arthritis, getting up in the morning can be hard.
o Joints may feel stiff and creaky for a short time, until get moving.
o May also get stiff from sitting.
The muscles around the joint may get weaker
o This happens a lot with arthritis in the knee.
Cracking and creaking
o Joints may make crunching, creaking sounds.
Limited range-of-motion
 X-RAY-although used for evaluating OA ,are
insensitive for identifying early disease
process. They correlate poorly with patients
symptom.
 Synovial fluid analysis-WBC’s count more than
1000/microlitre indicate inflammatory arthritis
and less likely OA.
 ULTRASOUND.
 MRI.
 CT-scan.
 BONE SCAN.
 CT-SCAN
OF HAND
SHOWING
OSTEOPHY
TE IN THE
HEAD OF
4TH
METACAR
PAL.
 RHEUMATOID A.
 Inflammatory.
 Symmetric involvement
of small joints first.
 Polyarticular.
 Other visceral organs
also affected.
 Erosion of adjuscent
bony surface.
 Morning stiffnes>1hr.
 OSTEOARTHRITIS
 Degenerative.
 Asymmetric
involvement of large
joint first.
 Generally
monoarticular.
 Not affected.
 Sclerosis of adjuscent
bony surface with
osteophyte formation.
 Morning stiffnes<1hr.
 A metabolic disease characterized by
recurrent attack of acute inflammatory
arthritis caused by elevated levels of uric
acid in the blood (hyperuricemia).
 Most common rheumatic disease of
adulthood
 The uric acid crystallizes and deposits in
joints, tendons, and surrounding tissues.
 Hyperuricemia :
overproduction/underexcretion/both
Hyperuricemia ≠ Gout
1. Acute gout
 Acute, self limiting, monoarticular
 Painful, red, hot, swollen
 Usually resolves within 2 weeks if untreated
 May occur even if serum urate is normal
 LL > UL
 Commonly affected joints
I. 1st metatarsophalangeal joint (podagra)
II. Forefoot/instep
III. Ankle joint
IV. Knee joint
V. Wrist joint
VI. Elbow joint
VII. Finger joints
 Extra-articular : olecranon bursa, Achilles tendon
 O/E : erythematous, warm, swelling over involved joint with
extreme tenderness +/- fever  skin desquamation
 Duration : 2 – 3 weeks, with gradual complete resolution of
inflammatory signs
2. Intercritical gout
 Asymptomatic period between attacks
3. Chronic gout
 Polyarticular arthritis + tophi formation
 Articular tophaceous gout may results in destructive
arthropathy and secondary OA
 Tophaceous disease more like to occur in patients with:
 Polyarticular presentation
 Serum urate level >540 μmol/L (>9mg/dL)
 Disease onset at younger age (≤40 years)
 Sites of tophi
 Digits of hands and feet (most common)
 Pinna of ear (classic, less common)
 Bursa around elbows and knees
 Achilles tendon
 Two of the following criteria are required
for clinical diagnosis :
1. Clear h/o at least 2 attacks of painful joint
swelling with complete resolution within 2
weeks
2. Clear history or observation of podagra
3. Presence of tophus
4. Rapid response to colchicine within 48 hours of
treatment initiation
 Definitive diagnosis : presence of
monosodium urate crystals seen in synovial
fluid/tissues
 Specific investigations for confirmation
 Serum uric acid
 Joint aspiration and crystal identification
 Not widely available
 To detect medical conditions a/w gout or hyperuricemia
 FBC
 Serum creatinine/urea
 Serum blood glucose
 Fasting lipid profile
 UFEME
 24h urinary urate excretion :
 Useful if renal calculus proven to be urate stone
 Indicated if on uricosuric agent
 Assess risk of stone
 Help to indicate whether overproduction or underexcretion of urate
 Range : 2-4 mmol/24h or 0.34-0.67g/24h
 To detect complications
 Renal imaging
 Skeletal x-rays
 Skeletal x-rays
 Acute gouty arthritis : normal; soft tissue
swelling
 Chronic tophaceous gout : tophi, erosive bone
lesions (punched out lesions), joint space is
preserved until late stage, pathognomonic in foot
and big toe
 Contributing factors eg. thiazide/loop
diuretics; low dose aspirin may be discontinued
or substituted, if appropriate
 Pharmacotherapy of asymptomatic
hyperuricemia is NOT necessary, except :-
 Persistent severe hyperuricemia
- > 770μmol/L (13mg/dL) in male
- > 600μmol/L (10mg/dL) in female
 Persistent elevated urinary excretion of urate
- > 0.65mmol/L/day (11mg/day), a/w 50% increased
risk of urate calculi
 Tumor lysis syndrome
- chemotherapy/radiotherapy  extensive tumor
cytolysis => require pre-hydration and allopurinol to
prevent acute urate nephropathy
 Initiation within 24 hours of onset
 If on Allopurinol, continue without interruption
 NSAIDs
 eg. Diclofenac, indomethacin, mefenemic acid etc
 Caution in h/o PUD, HPT, renal impairment, IHD, liver impairment
 COX-2 inhibitors (celecoxib, etoricoxib, parecoxib) = alternative for
above risk factors
 Studies have shown that etoxicoxib (Arcoxia) has equal efficacy to
indomethacin
 Colchicine
 Inhibiting mitosis and neutrophils motility and activity, leading to a
net anti-inflammatory effect.
 Alternative drug if CI to NSAIDs, but is poorly tolerated by elderly
 Therapeutic index is narrow
 Slower onset of action
 Evidence base for prophylaxis is stronger than for NSAIDs (NHS Fife, Gout
Management Guidelines, 2010)
 SE (eg. N&V, abd. pain, profuse diarrhea) limit its usefulness
 Dosage : 0.5mg – 0.6mg BD-QID
 Last resort for gouty arthritis
 Removal of tophi
 Joint fusion
 Joint replacement
 Ulceration of tophi : debridement, dressing
with sodium bicarbonate solution
 Indications for chronic tophaceous gout :
 Advanced tophi deposition resulting in major joint
destruction
 Loss of involved joint movements a/w severe pain
 Tophi collection causing pressure symptoms, eg
carpal tunnel syndrome of wrist
 Tophaceous ulcer
 Cosmetic eg ear lobe tophi
rheumatoid arthritis,gout & osteoarthritis

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rheumatoid arthritis,gout & osteoarthritis

  • 2.  Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease predominantly affecting diarthrodial joints and frequently a variety of other organs.  Peak incidence is between 4th and 6th decade.  Females are two to three times more affected than males.  Genetic and autoimmune factors are mainly responsible for the initiation of disease process.
  • 3. The pathologic hallmark of RA is synovial membrane proliferation and outgrowth associated with erosion of articular cartilage and subchondral bone. There is role of both cellular and humoral immune mechanism in the onset of inflammation.
  • 4.  Small joints of Hand-Pain/Stiffness > 1HR.  The pattern of joint involvement is typically polyarticular and symmetrical and involves-  proximal interphalangeal (PIP)  metacarpophalangeal (MCP)  wrist, elbow, shoulder, knee, ankle,MTP joints and cervical spine.  The distal interphalangeal (DIP) joints of the fingers are usually spared.
  • 5.
  • 6.  FEVER/MALAISE/HEADACHE  JOINT SWELLING/TENDERNESS.  With persistent inflammation, a variety of characteristic joint changes develop like-  Z-deformity  Swan neck deformity  Boutonniere deformity.
  • 7.
  • 8.  CLINICAL.  MRI IOC for early detection of disease  ULTRASOUND  X-RAYS.  CT SCAN.  SYNOVIAL FLUID ASPIRATION  ANEMIA,RAISED ESR…  SEROLOGICAL TESTS.
  • 9.  Guidelines for classification  a. Four of seven criteria are required to classify a patient as having rheumatoid arthritis (RA).  b. Patients with two or more clinical diagnoses are not excluded.
  • 10.  Criteria a. Morning stiffness: Stiffness in and around the joints lasting 1 h before maximal improvement. b. Arthritis of three or more joint areas: The 14 possible joint areas involved are right or left proximal interphalangeal, metacarpophalangeal, wrist, elbow, knee, ankle, and metatarsophalangeal joints.
  • 11. c. Arthritis of hand joints: Arthritis of wrist, metacarpophalangeal joint, or proximal interphalangeal joint. d. Symmetric arthritis: Simultaneous involvement of the same joint areas on both sides of the body. e. Rheumatoid nodules: Subcutaneous nodules over bony prominences, extensor surfaces, or juxtaarticular regions observed by a physician.
  • 12. f. Serum rheumatoid factor: Demonstration of abnormal amounts of serum rheumatoid factor. g. Radiographic changes: Typical changes of RA on posteroanterior hand and wrist radiographs that must include erosions or unequivocal bony decalcification localized in or most marked adjacent to the involved joints.
  • 13.
  • 14.
  • 15.  Most common type of arthritis.  Leading cause of disability in elderly.  Much more common in women than men.  Definition: OA is joint failure,a disease in which all parts of joint have undergone pathologic change.initial step in the onset of disease is failure of joint protective mechanism.  Joint vulnerability and joint loading are the two major factors in development of disease.
  • 16. Primary osteoarthritis is mostly related to aging. With aging, the water content of the cartilage increases, and the protein makeup of cartilage degenerates. Secondary osteoarthritis is caused by another disease or condition. Conditions that can lead to secondary osteoarthritis include obesity, repeated trauma or surgery to the joint structures, abnormal joints at birth (congenital abnormalities), gout, diabetes, and other hormone disorders.
  • 17.  Increasing age.  Female gender.  Obesity  Injurious physical activity.  Bridging muscle weakness.  Malalignment.  Proprioceptive deficiancies(eg.charcot arthropathy).  Genetic susceptibility.(hand and hip OA.)
  • 18.
  • 19.  Cartilage is the primary target tissue for OA.  There is nonuniform loss of the cartilage.  Evidense of new bone formation is presence of osteophytes.  There is as assymetric and nonuniform involvement of the joints.  Capsule may become edematous and fibrotic.  Joint space narrowing is present as seen in all types of arthritis.
  • 20.
  • 21.
  • 22. Symptoms Pain o Joints may ache, or the pain may feel burning or sharp. For some people, it may get better after a while. o Pain while sleeping or constant pain may be a sign that arthritis is getting worse. Stiffness o When you have arthritis, getting up in the morning can be hard. o Joints may feel stiff and creaky for a short time, until get moving. o May also get stiff from sitting. The muscles around the joint may get weaker o This happens a lot with arthritis in the knee. Cracking and creaking o Joints may make crunching, creaking sounds. Limited range-of-motion
  • 23.
  • 24.  X-RAY-although used for evaluating OA ,are insensitive for identifying early disease process. They correlate poorly with patients symptom.  Synovial fluid analysis-WBC’s count more than 1000/microlitre indicate inflammatory arthritis and less likely OA.  ULTRASOUND.  MRI.  CT-scan.  BONE SCAN.
  • 25.  CT-SCAN OF HAND SHOWING OSTEOPHY TE IN THE HEAD OF 4TH METACAR PAL.
  • 26.  RHEUMATOID A.  Inflammatory.  Symmetric involvement of small joints first.  Polyarticular.  Other visceral organs also affected.  Erosion of adjuscent bony surface.  Morning stiffnes>1hr.  OSTEOARTHRITIS  Degenerative.  Asymmetric involvement of large joint first.  Generally monoarticular.  Not affected.  Sclerosis of adjuscent bony surface with osteophyte formation.  Morning stiffnes<1hr.
  • 27.
  • 28.  A metabolic disease characterized by recurrent attack of acute inflammatory arthritis caused by elevated levels of uric acid in the blood (hyperuricemia).  Most common rheumatic disease of adulthood  The uric acid crystallizes and deposits in joints, tendons, and surrounding tissues.  Hyperuricemia : overproduction/underexcretion/both Hyperuricemia ≠ Gout
  • 29. 1. Acute gout  Acute, self limiting, monoarticular  Painful, red, hot, swollen  Usually resolves within 2 weeks if untreated  May occur even if serum urate is normal  LL > UL  Commonly affected joints I. 1st metatarsophalangeal joint (podagra) II. Forefoot/instep III. Ankle joint IV. Knee joint V. Wrist joint VI. Elbow joint VII. Finger joints  Extra-articular : olecranon bursa, Achilles tendon  O/E : erythematous, warm, swelling over involved joint with extreme tenderness +/- fever  skin desquamation  Duration : 2 – 3 weeks, with gradual complete resolution of inflammatory signs
  • 30. 2. Intercritical gout  Asymptomatic period between attacks 3. Chronic gout  Polyarticular arthritis + tophi formation  Articular tophaceous gout may results in destructive arthropathy and secondary OA  Tophaceous disease more like to occur in patients with:  Polyarticular presentation  Serum urate level >540 μmol/L (>9mg/dL)  Disease onset at younger age (≤40 years)  Sites of tophi  Digits of hands and feet (most common)  Pinna of ear (classic, less common)  Bursa around elbows and knees  Achilles tendon
  • 31.  Two of the following criteria are required for clinical diagnosis : 1. Clear h/o at least 2 attacks of painful joint swelling with complete resolution within 2 weeks 2. Clear history or observation of podagra 3. Presence of tophus 4. Rapid response to colchicine within 48 hours of treatment initiation  Definitive diagnosis : presence of monosodium urate crystals seen in synovial fluid/tissues
  • 32.  Specific investigations for confirmation  Serum uric acid  Joint aspiration and crystal identification  Not widely available  To detect medical conditions a/w gout or hyperuricemia  FBC  Serum creatinine/urea  Serum blood glucose  Fasting lipid profile  UFEME  24h urinary urate excretion :  Useful if renal calculus proven to be urate stone  Indicated if on uricosuric agent  Assess risk of stone  Help to indicate whether overproduction or underexcretion of urate  Range : 2-4 mmol/24h or 0.34-0.67g/24h  To detect complications  Renal imaging  Skeletal x-rays
  • 33.  Skeletal x-rays  Acute gouty arthritis : normal; soft tissue swelling  Chronic tophaceous gout : tophi, erosive bone lesions (punched out lesions), joint space is preserved until late stage, pathognomonic in foot and big toe
  • 34.  Contributing factors eg. thiazide/loop diuretics; low dose aspirin may be discontinued or substituted, if appropriate  Pharmacotherapy of asymptomatic hyperuricemia is NOT necessary, except :-  Persistent severe hyperuricemia - > 770μmol/L (13mg/dL) in male - > 600μmol/L (10mg/dL) in female  Persistent elevated urinary excretion of urate - > 0.65mmol/L/day (11mg/day), a/w 50% increased risk of urate calculi  Tumor lysis syndrome - chemotherapy/radiotherapy  extensive tumor cytolysis => require pre-hydration and allopurinol to prevent acute urate nephropathy
  • 35.  Initiation within 24 hours of onset  If on Allopurinol, continue without interruption  NSAIDs  eg. Diclofenac, indomethacin, mefenemic acid etc  Caution in h/o PUD, HPT, renal impairment, IHD, liver impairment  COX-2 inhibitors (celecoxib, etoricoxib, parecoxib) = alternative for above risk factors  Studies have shown that etoxicoxib (Arcoxia) has equal efficacy to indomethacin  Colchicine  Inhibiting mitosis and neutrophils motility and activity, leading to a net anti-inflammatory effect.  Alternative drug if CI to NSAIDs, but is poorly tolerated by elderly  Therapeutic index is narrow  Slower onset of action  Evidence base for prophylaxis is stronger than for NSAIDs (NHS Fife, Gout Management Guidelines, 2010)  SE (eg. N&V, abd. pain, profuse diarrhea) limit its usefulness  Dosage : 0.5mg – 0.6mg BD-QID
  • 36.  Last resort for gouty arthritis  Removal of tophi  Joint fusion  Joint replacement  Ulceration of tophi : debridement, dressing with sodium bicarbonate solution  Indications for chronic tophaceous gout :  Advanced tophi deposition resulting in major joint destruction  Loss of involved joint movements a/w severe pain  Tophi collection causing pressure symptoms, eg carpal tunnel syndrome of wrist  Tophaceous ulcer  Cosmetic eg ear lobe tophi